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Activation of the cold-sensing TRPM8 channel triggers UCP1-dependent thermogenesis and prevents obesity.

Authors: Ma, Shuangtao  Yu, Hao  Zhao, Zhigang  Luo, Zhidan  Chen, Jing  Ni, Yinxing  Jin, Rongbing  Ma, Liqun  Wang, Peijian  Zhu, Zhenyu  Li, Li  Zhong, Jian  Liu, Daoyan  Nilius, Bernd  Zhu, Zhiming 
Citation: Ma S, etal., J Mol Cell Biol. 2012 Apr;4(2):88-96. doi: 10.1093/jmcb/mjs001. Epub 2012 Jan 11.
Pubmed: (View Article at PubMed) PMID:22241835
DOI: Full-text: DOI:10.1093/jmcb/mjs001

Brown adipose tissue (BAT) is an energy-expending organ that produces heat. Expansion or activation of BAT prevents obesity and diabetes. Chronic cold exposure enhances thermogenesis in BAT through uncoupling protein 1 (UCP1) activation triggered via a ß-adrenergic pathway. Here, we report that the cold-sensing transient receptor potential melastatin 8 (TRPM8) is functionally present in mouse BAT. Challenging brown adipocytes with menthol, a TRPM8 agonist, up-regulates UCP1 expression and requires protein kinase A activation. Upon mimicking long-term cold exposure with chronic dietary menthol application, menthol significantly increased the core temperatures and locomotor activity in wild-type mice; these effects were absent in both TRPM8(-/-) and UCP1(-/-) mice. Dietary obesity and glucose abnormalities were also prevented by menthol treatment. Our results reveal a previously unrecognized role for TRPM8, suggesting that stimulation of this channel mediates BAT thermogenesis, which could constitute a promising way to treat obesity.


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RGD Object Information
RGD ID: 13673845
Created: 2018-06-23
Species: All species
Last Modified: 2018-06-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.